AIR QUALITY CRITERIA
FOR
PHOTOCHEMICAL OXIDANTS
SUMMARY AND CONCLUSIONS
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
Public Health Service
Environmental Health Service
-------
3
AIR QUALITY CRITERIA
FOR
PHOTOCHEMICAL OXIDANTS
(The summary and conclusions herein
are reproduced from the original
volume as identified on this page.)
US EPA
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^ U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
Public Health Service
Environmental Health Service
National Air Pollution Control Administration
Washington, D.C.
March 1970
Repository Material
!annanent Collection
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Chapter 10.
SUMMARY AND CONCLUSIONS
A. INTRODUCTION
This document is a consolidation and
assessment of the current state of knowledge
on the origin and effects of the group of air
pollutants known as photochemical oxidants
on health, vegetation, and materials. The
purpose of this chapter is to provide a concise
picture of the information contained in this
document, including conclusions which are
believed reasonable to consider in evaluating
concentrations of photochemical oxidants
which are known to have an effect on either
health or welfare. Although nitrogen dioxide
is considered one of the photochemical
oxidants, it is to be subject of a separate
report. Consequently, nitrogen dioxide is
discussed in this document only to the extent
that it participates in the formation and reac-
tions of other photochemical oxidants. The
information and data contained in this docu-
ment comprise the best available bases, and
provide the rationale for development of
specific levels of standards of photochemical
oxidants in the ambient ah- for protection of
public health and man's environment.
B. NATURE OF PHOTOCHEMICAL
OXIDANTS
Photochemical oxidants result from a com-
plex series of atmospheric reactions initiated
by sunlight. When reactive organic substances
and nitrogen oxides accumulate in the atmo-
sphere and are exposed to the ultraviolet
component of sunlight, the formation of new
compounds, including ozone and peroxyacyl
nitrates, takes place.
Absorption of ultraviolet light energy by
nitrogen dioxide results in its dissociation into
nitric oxide and an oxygen atom. These
oxygen atoms for the most part react with air
oxygen to form ozone. A small portion of the
oxygen atoms and ozone react also with
certain hydrocarbons to form free radical
intermediates and various products. In some
complex manner, the free radical intermedi-
ates and ozone react with the nitric oxide
produced initially. One result of these reac-
tions is the very rapid oxidation of the nitric
oxide to nitrogen dioxide and an increased
concentration of ozone.
The photochemical system generally is ca-
pable of duplication in the laboratory. For
various reasons, however, laboratory results
cannot be quantitatively extrapolated to the
atmosphere. Theoretically generation of an
atmospheric simulation model should be feasi-
ble, enabling the prediction of ambient oxi-
dant concentrations from a knowledge of
emission and meteorological data. The devel-
opment of such a model, however, is depen-
dent on the acquisition of more reliable and
applicable quantitative information derived
from direct atmospheric observations, as well
as on the refinement of results obtained from.
irradiation chamber studies.
C. ATMOSPHERIC PHOTOCHEMICAL
OXIDANT CONCENTRATIONS
The presence of photochemically formed
oxidants has been indicated in all of the major
U.S. cities for which aerometric data have
been examined. On a concentration basis,
ozone has been identified as the major com-
ponent of the oxidant levels observed. Diffi-
culties arise, however, in interpreting data
obtained by the most commonly used oxidant
measuring method; this method is nonspecific
and subject to several interferences. Adjusted
oxidant concentrations, obtained by correc-
ting potassium iodide oxidant measurements
10-1
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for known interferences, have been found to
be relatively close to concurrent measure-
ments of ozone alone.
Since photochemical oxidants are the pro-
ducts of atmospheric chemical reactions, the
relationship between precursor emissions and
atmospheric oxidant concentrations is much
less direct than is the case for primary
pollutants. A further complicating situation is
the dependence of these photochemical reac-
tions on intensity and duration of sunlight,
and on temperature.
In an analysis of oxidant concentration
data for 4 years and 12 stations, the daily
maximum 1-hour average concentration was
equal to or exceeded 290 jug/m3 (0.15 ppm)
up to 41 percent of the time; maximum
1-hour average concentrations ranged from
250 to 1,140 jug/™3 (0.13 to 0.58 ppm);
short-term peaks were as high as 1,310 jug/™3
(0.67 ppm). Yearly averages, commonly app-
lied to other pollutants, are not representative
of air quality with respect to oxidant pollu-
tion, because 1-hour average ozone concentra-
tions will necessarily be at or about zero for
approximately 75 percent of the time when
photochemical reactions are minimal.
Peroxyacyl nitrates, through not routinely
measured, have been identified in the atmo-
sphere of several cities. These compounds
may be assumed to be present whenever
oxidant levels are elevated.
D. NATURAL SOURCES OF OZONE
Ozone can be formed naturally in the
atmosphere by electrical discharge, and in the
stratosphere by solar radiation, by processes
which are not capable of producing signifi-
cant urban concentrations of this pollutant.
Maximum instantaneous ozone levels of from
20 to 100 /ig/m3 (0.01 to 0.05 ppm) have
been recorded in nonurban areas.
E. MEASUREMENT OF PHOTOCHEMICAL
OXIDANTS
The most widely used technique for the
analysis of atmospheric total oxidants is based
on the reaction of these compounds with
potassium iodide to release iodine. The iodine
may then be measured by either colorimetnc
or coulometric methods. Calibrating the oxi-
dant measurement method used against a
known quantity of ozone provides a measure-
ment of the net oxidizing properties of the
atmosphere in terms of an equivalent concen-
tration of ozone. Most oxidant measurements
are currently being made by the colorimetric
method, although coulometric analyzers are
used in a number of laboratory and field studies.
In order to generate comparable data, it is
essential that all measurements be made by
techniques which have been calibrated against
the same standard or reference method. Since
at the present time there is no standard
method for the determination of total oxi-
dants, the National Air Pollution Control
Administration recommends use of the neu-
tral-buffered 1 percent potassium iodide col-
orimetric technique as the method against
which all instruments and other methods
should be compared. In addition to serving as
a manual procedure for determining oxidants,
the reference method may be used in conjunc-
tion with a "dynamic calibration" technique
for instrumental methods.
Reducing agents such as sulfur dioxide
produce a negative interference in oxidant
determination. Such interference can be re-
duced, however, by passing the air stream
through a chromium trioxide scrubber prior
to measurement. Unfortunately, a portion of
the nitric oxide which may be present in the
air stream is oxidized to nitrogen dioxide by
the scrubber. This results in an apparent
increase in the oxidant measurement of about
11 percent of the concentration of nitric
oxide. Moreover, a portion of the atmospher-
ic nitrogen dioxide concentration will also
contribute to the oxidant measurement. Per-
oxyacyl nitrate concentrations are usually
small and contribute only a very slight
amount to the oxidant reading.
There are several means for the specific
measurement of atmospheric ozone. Instru-
mental methods include chemiluminescent
analysis based on the reaction of ozone with
Rhodamine B, gas phase olefin titration, and
10-2
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ultraviolet and infrared spectroscopy. A semi-
quantitative method for ozone measurement
is based on its ability to produce cracks in
stretched rubber. Peroxyacyl nitrates can be
measured in the atmosphere by gas chromato-
graphy with the use of an electron-capture
detector.
For a better evaluation of the results of
research on the effects of photochemical
oxidants, it is essential that data be obtained
for individual oxidants such as nitrogen diox-
ide, ozone, PAN, formaldehyde, acrolein, and
organic peroxides. These data would either
replace or complement data on total oxidants.
Instrumentation currently available permits
the accurate measurement of atmospheric
ozone, nitrogen dioxide, and PAN. There
exists, however, a further need to develop
instruments capable of measuring other indi-
vidual gaseous pollutants which have the
properties of oxidants. Photochemical reac-
tions and problems derived from oxidants can
be much better defined using specific meth-
ods for measurement in preference to the
traditional total oxidants determination.
F. EFFECTS OF PHOTOCHEMICAL
OXIDANTS ON VEGETATION
AND MICROORGANISMS
Injury to vegetation is one of the earliest
manifestations of photochemical air pollu-
tion, and sensitive plants are useful biological
indicators of this type of pollution. The
visible symptoms of photochemical oxidant
produced injury to plants may be classified
as: (1) acute injury, identified by cell collapse
with subsequent development of necrotic
patterns; (2) chronic injury, identified by
necrotic patterns with or without chlorotic or
other pigmented patterns; and, (3) phsyiologi-
cal effects, identified by growth alterations,
reduced yields, and changes in the quality of
plant products. The acute symptoms are
generally characteristic of a specific pollutant;
though highly characteristic, chronic injury
patterns are not. Ozone injury to leaves is
identified as a stippling or flecking. Such
injury has occurred experimentally in the
most sensitive species after exposure to 60
jug/m3 (0.03 ppm) ozone for 8 hours. Injury
will occur in shorter time periods when low
levels of sulfur dioxide are present. PAN-pro-
duced injury is characterized by an under-sur-
face glazing or bronzing of the leaf. Such
injury has occurred experimentally in the
most sensitive species after exposure to 50
jug/m3 (0.01 ppm) PAN for 5 hours. Leaf
injury has occurred in certain sensitive species
after a 4-hour exposure to 100 jig/m3 (0.05
ppm) total oxidant. Ozone appears to be the
most important phytotoxicant in the photo-
chemical complex.
There are a number of factors affecting the
response of vegetation to photochemical air
pollutants. Variability in response is known to
exist between species of a given genus and
between varieties within a given species; varie-
tal variations have been most extensively
studied with tobacco. The influence of light
intensity on the sensitivity of plants to damage
during growth appears to depend on the phy-
totoxicant. Plants are more sensitive to PAN
when grown under high light intensities, but
are more sensitive to ozone when grown under
low light intensities. Reported findings are in
general agreement that sensitivity of green-
house-grown plants to oxidants increases with
temperature, from 10° to 38° C (40° to 100°
F), but this positive correlation may result
from the overriding influence of light intensi-
ty on sensitivity. The effects of humidity on
the sensitivity of plants has not been well
documented. General trends indicate that
plants grown and/or exposed under high
humidities are more sensitive than those
grown at low humidities. There has been little
research in this direction, but there are
indications that soil factors such as drought
and total fertility influence the sensitivity of
plants to phytotoxic air pollutants. The age of
the leaf under exposure is important in de-
termining its sensitivity to air pollutants.
There is some evidence that oxidant or ozone
injury may be reduced by pretreatment with
the toxicant.
10-3
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Identification of injury to a plant as being
caused by air pollution is a difficult undertak-
ing. Even when the markings on the leaves of
a plant may be identified with an air pollut-
ant, there is the further difficulty of evaluat-
ing the injury in terms of its effect on the
intact plant. Additional problems arise in
trying to evaluate the economic impact of
air pollution damage to a plant.
The interrelations of time and concen-
tration (dose) as they affect injury to plants
are essential to air quality criteria. There are,
however, only scant data relating concen-
trations and length of photochemical oxi-
dant exposure to chronic injury and effects
on reduction of plant growth, yield, or
quality. There is also a dearth of infor-
mation relating concentrations to acute
injury. A larger body of information exists
on the acute effects of ozone, but even in
this instance, the information is far from
complete. Sufficient data do exist, however,
to tabularly present ozone concentrations
which will produce 5 percent injury to sensi-
tive, intermediate, and resistant plants after
a given short-term exposure, as shown in
Table 10-1. Information available lists 20
species and/or varieties as sensitive, 55 as
intermediate in sensitivity, and 64 as rela-
tively resistant.
Bacteriostatic and bacteriocidal properties
of photochemical oxidants in general have
been demonstrated. The growth suppression
of microorganisms by ozone is a well-known
phenomenon, although the ozone concen-
trations for this activity are undesirable from
a human standpoint. The bacteriocidal
activity of ozone varies with its concen-
tration, the relative humidity, and the
species of bacteria.
G. EFFECT OF OZONE ON MATERIALS
The detailed, quantitative extent of damage
to materials caused by atmospheric levels of
ozone is unknown, but generally any organic
material is adversely affected by concentrated
ozone. Many polymers are extremely sensitive
to even very small concentrations of ozone,
this sensitivity increasing with the number of
double bonds in the structure of the polymer.
Economically, rubber is probably the most
important material sensitive to ozone attack,
particularly styrene-butadiene, natural, poly-
butadiene, and synthetic polyisoprene. Anti-
ozonant additives have been developed and
are capable of protecting elastomers from
ozone degradation; synthetic rubbers with
inherent resistance to ozone are also available.
These additives are expensive, however, and
add to the cost of the end product; in
addition, increasing amounts of antiozonants
are required as the amount of ozone which is
to be encountered increases, and sometimes
only temporary protection is provided.
Ozone attacks the cellulose in fabrics
through both a free radical chain mechanism
and an electrophilic attack on double bonds;
light and humidity appear necessary for ap-
preciable alterations to occur. The relative
susceptibility of different fibers to ozone
attack appears to be, in increasing order,
cotton, acetate, nylon, and polyester.
Table 10-1. PROJECTED OZONE CONCENTRATIONS WHICH WILL PRODUCE, FOR
SHORT-TERM EXPOSURES, 5 PERCENT INJURY TO ECONOMICALLY
IMPORTANT VEGETATION GROWN UNDER SENSITIVE CONDITIONS
Time,
hi
0.2
0.5
1.0
2.0
4.0
8.0
Ozone concentrations producing injury in three types of plants, ppm
Sensitive
0.35-0.75
0.15-0.30
0.10-0.25
0.07-0.20
0.05-0.15
0.03-0.10
Intermediate
0.70-1.00
0.25-0.60
0.20-0.40
0.15-0.30
0.10-0.25
0.08-0.20
Resistant
0.90 and up
0.50 and up
0.35 and up
0.25 and up
0.20 and up
0.15 and up
10-4
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Certain dyes are susceptible to fading during
exposure to ozone. The rate and extent of fad-
ing is also dependent upon other environmental
factors such as relative humidity and the
presence of air pollutants other than ozone, as
well as the length and concentration of ozone
exposure and the type of material exposed.
H. TOXICOLOGICAL STUDIES OF
PHOTOCHEMICAL OXIDANTS
1. Effects of Ozone in Animals
The major physiological effects of ozone
are on the respiratory system. Inhalation of
ozone at concentrations greater than about
5,900 pg/m3 (3 ppm) for several hours pro-
duces hemorrhage and edema in the lungs.
This reaction can be fatal to animals. Rats and
mice appear to be more sensitive than rabbits,
cats, and guinea pigs. The toxicity is greater
for young animals and for exercising animals.
It is abated by intermittency of exposure, by
prophylactic administration of chemical re-
ducing agents, or by introducing agents into
the diet which reduce the activity of the
thyroid gland. At exposures less than those
which produce edema in the lungs, changes in
the mechanical properties of the lung occur.
These are accompanied by increased breathing
rates and increased oxygen consumption. Re-
peated non-fatal exposures to concentrations
greater than 15,700 jug/m3 (8 ppm) for 30
minutes have produced fibrosis in the respira-
tory tract of rabbits, with the damage increas-
ing in severity over the length of the respira-
tory tract from the trachea to the bronchioles.
Short-term exposures to ozone also pro-
duce chemical changes in the lung tissue ele-
ments of animals. A study conducted on a
small number of rabbits showed that inhala-
tion of 1,960 to 9,800 Mg/m3 (1 to 5 ppm)
ozone for 1 hour can produce denaturation of
the structural lung proteins. Ozone also ap-
pears to oxidize the sulfhydryl groups of
amino acids in the lung.
Short-term exposures to ozone also pro-
duce changes in organs other than the lung.
Concentrations of 5,900 jug/m3 (3 ppm) for
20 hours can stimulate some adaptive liver
enzymes. Inhalation of 390 to 490
(0.2 to 0.25 ppm) ozone for 30 to 60 minutes
makes the red blood cells of mice, rabbits,
rats, and man more sensitive to the shape-al-
tering effects of' irradiation. Exposure of
blood to ozone in vitro produces interference
with the release of oxygen from red blood
cells; this suggests that ozone exposure could
impair the delivery of oxygen to the tissues.
Ozone exposures at concentrations from
1,310 to 7,800 jug/m3 (0.67 to 4.0 ppm) have
been shown to reduce the in vitro phagocytic
abilities of the pulmonary alveolar macrophag-
es. A 3-hour exposure to 9,800 jug/m3 (5
ppm) ozone has been shown to reduce the
activity of bactericidal enzyme, presumably
due to in vivo oxidation of the enzyme.
Ozone inhalation increases the vulnerability
of animals to other agents. A single exposure
to ozone at a concentration of 160 jug/m3
(0.08 ppm) for 3 hours has increased the
mortality among mice from inhalation of
pathogenic bacteria. This occurred when the
bacteria were administered both before and
after exposure to ozone. Ozone also increases
the toxicity of histamine in guinea pigs.
Long-term effects of ozone exposure in-
clude, in some species, the development of
tolerance to biological effects of ozone,
production of fibrotic changes in the lungs,
and a possible increase in the rate of aging.
While tolerance has been shown in rodents, it
has not been shown in chickens, and it is not
certain whether or not it occurs in man. In
species where tolerance to ozone exposure has
been demonstrated, information is not avail-
able concerning the duration and mechanism
of tolerance following repeated exposure. The
aging effect may be similar to the changes
produced by exposure to free radicals or by
irradiation.
2. Effects of Ozone in Humans
Some studies of human exposures to ozone
have focused on the determination of the
threshold level at*which odor can be detected,
and on the occurrence of changes in pulmo-
nary function. Nine out of 10 subjects ex-
posed to 40 pig/m3 (0.02 ppm) ozone were
able to detect the odor immediately, and it
10-5
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persisted for an average of 5 minutes. Thir-
teen of 14 subjects exposed to 100 pg/m3
(0.05 ppm) ozone indicated the odor is
considerably stronger at this concentration,
and the odor persisted for an average of 13
minutes.
Occupational exposure of humans to ozone
concentrations of up to 490 jug/m3 (0.25
ppm) has not produced detectable changes in
pulmonary function. Respiratory symptoms
and a decrease in vital capacity in three out of
seven smokers who had been occupationally
exposed to ozone have occurred at concentra-
tions greater than 590 jug/m3 (0.3 ppm).
Experimental exposures of humans have
been carried out at concentrations ranging
from 200 to 7,800 /ug/m3 (0.1 to about 4
ppm) for periods of up to 2 hours. Exposure
to 390 ng/m3 (0.2 ppm) for 3 hours daily, 6
days a week, for 12 weeks has not produced
any change in ventilatory function tests.
Similar exposure to 980 jug/m3 (0.5 ppm)
produced a decrease in the forced expiratory
volume during the last 4 weeks of exposure,
with recovery taking place in a subsequent
6-week period. In each of 11 subjects, expo-
sure to 1,180 to 1,570 jug/m3 (0.6 to 0.8
ppm) for 2 hours resulted in an impairment of
the diffusing capacity of the lung. Small
decreases in vital capacity and forced expira-
tory volume were observed in some of these
subjects. Resistance to flow of air in the
respiratory tract increased slightly in some sub-
jects after exposure to 200 to 1,180 /ug/m3
(0.1 to 0.6 ppm) for 1 hour, and increased con-
sistently in each of four subjects after exposure
to 1,960 Mg/m3 (1 ppm) for 1 hour.
Data obtained from animal experimenta-
tion cannot be used directly to define the
ozone concentrations above which human
health will be affected. Animal mortality
studies, however, can be useful in determining
the factors involved in toxicity. While the
concentrations of ozone used in the deter-
mination of short-term non-fatal effects in
animals are rarely found in ambient air, the
changes in pulmonary function observed dur-
ing and after exposure to these concentrations
call attention to the possibility that similar
effects may be observed in humans.
When interpreting the research conducted
thus far using human subjects, it must be
noted that occupational exposures differ from
experimental exposures, because it is difficult
in an occupational environment to define the
exact nature and dose of the pullutants
present.
3. Effects of Peroxyacetyl Nitrate
Experimental studies with peroxyacetyl ni-
trate (PAN) in animals indicate that mortality
may be delayed for 7 to 14 days after
exposure; however, the exposure levels requir-
ed to produce this mortality never occur in
ambient atmospheres.
A single experimental study of healthy
human subjects exposed to 1,485 jug/m3 (0.3
ppm) peroxyacetyl nitrate indicated only that
there may be a small increase in oxygen
uptake with exercise. Sensitive pulmonary
function tests were not obtained.
The data from animal and human studies
are sparse and inadequate for determining the
toxicological potential of peroxyacetyl ni-
trate. It would appear, however, that at the
concentrations of this compound known to
occur in ambient atmospheres, PAN does not
present any recognized health hazard.
4. Effects of Mixtures Containing Photo-
chemical Oxidants on Animals
Studies have been conducted on animals
exposed to both synthetic and natural photo-
chemical smog. Synthetic smog has been
produced by the irradiation of diluted motor
vehicle exhaust or by irradiation of air mix-
tures containing nitrogen oxides and certain
hydrocarbons. Exposures to irradiated motor
vehicle exhaust are complicated by the simul-
taneous presence of carbon monoxide and
other non-oxidant substances which include
high concentrations of formaldehyde. Guinea
pigs show increased respiratory volume during
a four-hour exposure to irradiated exhaust
containing 1,570 /ig/m3 (0.8 ppm) total
oxidant.
10-6
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Exposure of mice to both natural and
synthetic smog for 3 hours, at concentrations
greater than 780 Mg/m3 (0.4 ppm) oxidants
have produced changes in the fine structure of
the lung. The nature and extent of the
damage was the same after exposure to either
type of smog with the same oxidant levels.
The severity of the damage increased with age
and became irreversible at age 21 months.
Chronic exposure of guinea pigs to ambient
air with an average oxidant concentration of
from 40 to 140 Mg/m3 (0.02 to 0.07 ppm)
leads to a significant increase in flow resist-
ance when the peak oxidant concentrations
exceed 980 Mg/m3 (0-5 ppm).
When male mice, prior to mating, were
given long-term exposures to irradiated auto
exhaust containing from 200 to 1,960 /-tg/m3
(0.1 to 1.0 ppm) oxidant, a decrease in
fertility and an increase in neonatal mortality
of their offspring resulted; the irradiated
mixture also contained varying concentrations
of carbon monoxide, nitrogen oxides, and
hydrocarbons. Similar exposures also cause a
reduction in spontaneous running activity,
which results in an adaptation response.
Thus a number of experimental studies
have demonstrated that changes in lung tissue
or lung function occur when animals are
exposed for several hours to photo-oxidized
mixtures containing 980 Mg/m3 (0.5 ppm) or
more of oxidants.
5. Effects of Mixtures Containing Photo-
chemical Oxidants on Humans
Laboratory studies of human exposure to
photochemical smog have involved primarily
the measurement of eye irritation. Based on
the existing data, it appears that: (1) the
effective eye irritants are the products of
photochemical reactions; (2) although oxi-
dant concentrations may correlate with the
severity of eye irritation, a direct cause-effect
relationship has not been demonstrated since
ozone, the principal contributor to ambient
oxidant levels is not an eye irritant; (3) the
precursors of the eye irritants are organic
compounds in combination with oxides of
nitrogen, the most potent being aromatic
hydrocarbons; (4) the chemical identities of
the effective irritants in synthetic systems are
known as being formaldehyde, peroxybenzoyl
nitrate (PBzN), peroxyacetyl nitrate (PAN),
and acrolein, although the latter two contri-
bute to only a minor extent; and (5) the
substances causing eye irritation in the atmo-
sphere have not been competely defined.
I. EPIDEMIOLOGICAL STUDIES OF PHO-
TOCHEMICAL OXIDANTS
Several studies have examined daily mortal-
ity rates in localities where photochemical air
pollution occurs, to determine if a relation-
ship exists with increased levels of oxidant.
Such an association has not been shown.
These studies, however, pose a number of
unresolved questions. One of these is, what is
the effect of temperature, either alone or in
combination with oxidants? In some of the
most severe episodes, there has been an
associated increase in environmental tempera-
ture, sufficient to cause excess mortality by
itself. Several studies of mortality among resi-
dents in nursing homes in Los Angeles showed
such excess mortality. In recent heat wave
and air pollution episodes, however, large
proportions of the elderly and ill persons in
nursing homes have been protected by air
conditioning.
Evidence of increased morbidity has been
sought through study of general hospital
admissions, but no unequivocal association
between photochemical air pollution and in-
creased morbidity has been shown. Additional
studies are indicated for improved definition.
Peak oxidant values of 250 //g/m3 (0.13
ppm), which might be expected in relation to
maximum hourly average levels of 100 to 120
/jg/m3 (0.05 to 0.06 ppm), have been associa-
ted with aggravation of asthma. No associa-
tion between ambient oxidant concentrations
and changes in respiratory symptoms or func-
tion was shown, however, in two separate
studies of subjects with preexisting chronic
respiratory disease. Non-smoking subjects
with chronic respiratory disease did, however,
demonstrate less airway resistance when they
were studied in a room where the ambient air
10-7
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of Los Angeles was filtered before entry. No
acute or chronic effects of oxidant pollution
on ventilatory performance of elementary
schoolchildren were demonstrated in a study
conducted in two communities within the Los
Angeles basin.
Impairment of performance by high school
athletes has been observed when photochemi-
cal oxidants ranged from 60 to 590 /ug/m3
(0.03 to 0.3 ppm) for 1 hour immediately
prior to the start of activities. Significantly,
more automobile accidents have also occurred
on days of high oxidant concentrations, but
no threshold level for this effect could be
determined from the analysis.
Among the general community, eye irrita-
tion is a major effect of photochemical air
pollution. In Southern California, it has af-
fected more than three-fourths of the popula-
tion. Eye irritation under conditions prevalent
in Los Angeles is likely to occur in a large
fraction of the population when oxidant
concentrations in ambient air increases to
about 200 jug/m3 (0.10 ppm). This oxidant
value might be expected to be associated with
a maximum hourly average oxidant concen-
tration of 50 to 100 Mg/m3 (0.025 to 0.50
ppm), depending on localized conditions.
According to survey data gathered in 1956,
asthma, cough, and nose and throat com-
plaints were more frequent in Los Angeles,
Orange, and San Diego counties than in the
San Francisco Bay area or in the rest of the
State.
Casual reports of the presence of the
symptoms of eye irritation have been record-
ed in many cities in the United States.
Epidemiologic studies have been inadequate,
however, to relate these symptoms clearly to
measured exposures to photochemical oxi-
dants. In fact, one of the major photochemi-
cal oxidants, ozone, is not an eye irritant.
That eye irritation is experienced whenever
the oxidant level exceeds a certain value is an
indication that oxidant concentrations corre-
late well with other aspects of the photo-
chemical complex; oxidant levels are probably
a measure of the photochemical activity
which produces the eye irritants. On the other
hand, it must be recognized that reactions of
ozone with hydrocarbons do lead to hydro-
carbon fragments which are eye irritants. Nor
can the possibility be discounted that ozone
in the photochemical complex may exert a
synergistic effect on eye irritation. Because
the oxidant reading measured only the net
oxidizing property of the atmosphere, how-
ever, the same amount of eye irritation
experienced in two different geographical
locations from identical irritants could be
associated with different levels of oxidant, if
other pollutants differed in their concentra-
tion.
J. AREAS FOR FUTURE RESEARCH
1. Environmental Aspects of Photochemical
Oxidants
1. Research should be conducted to further
identify the substance(s) which cause
eye irritation.
2. The nature of the photochemical aero-
sol, its behavior at different pressures of
water vapor, and the nature of the
surface layer of the particulates remains
to be determined.
3. The role of sulfur dioxide in the forma-
tion of photochemical aerosols and in
the impairment of visibility should be
investigated.
4. Mechanisms of photochemical oxidant
formation should be explained.
2. Toxicity of Ozone, Photochemical
Oxidants, and Peroxyacyl Nitrates
l.The effect of ozone and PAN in
combination with other pollutants found
in ambient air should be investigated.
Considerable information is available on
the separate effects of ozone, nitrogen
dioxide, and sulfur dioxide, but data on
the combined effects of defined concen-
trations of these gases are sparse. The
effect of particulates (dust, saline drop-
lets, oil, soots, etc.) should be deter-
mined alone and in combination with
the gases. Additional variables such as
10-8
-------
humidity and temperature should be
controlled and recorded. These experi-
ments should be carried out with materi-
als, vegetation, animals, and, under ap-
propriate conditions, in man.
2. Experiments with human exposures to
gas mixtures should include a compari-
son between the respiratory effects
shown in healthy subjects and those
shown in patients with chronic respira-
tory disease, care being taken to respect
the rights of experimental subjects.
3. Existing data demonstrate that tolerance
occurs only in rodents. Indices other
than mortality are required to demon-
strate tolerance in animals. If such in-
dices can be developed, then a study is
needed to see if a similar phenomenon
occurs in man.
4. The mechanisms of systemic effects of
ozone (headache, fatigue, impaired oxy-
gen transport by hemoglobin, inability
to concentrate, etc.) have yet to be
explained.
5. The rate and site of uptake of ozone and
its fate following uptake should be deter-
mined in vegetation and animals.
6. The mechanism for the production of
ozone-induced pulmonary edema re-
mains unexplained.
7. Additional research in needed to define
the role of peroxyacyl nitrates in the
production of eye irritation.
3. Epidemiology of Photochemical Oxidants
1. Of high priority is the need to study eye
and respiratory irritation in metropolitan
areas outside of California. Studies
should be supplemented by pulmonary
function tests.
2. Although the effects of episodes of high
pollution levels have been studied with
respect to mortality, morbidity, impair-
ment of performance, etc., additional
studies are needed at different sites and
for different effects. These should in-
clude congenital malformations, still-
births, hospitals admissions for miscar-
riage, and alterations in the sex ratio of
newborns.
3. The examination of children has received
insufficient attention in epidemiologic
studies of the health effects of air
pollution. This should be undertaken
with respect to the effects of photo-
chemical oxidants using simple pulmon-
ary function tests. Emphasis should be
placed on further studies of the inci-
dence of asthma attacks during episodes
of high pollution.
K. CONCLUSIONS
Derived from a careful evaluation of the
studies cited in this document, the conclu-
sions given below represent the best judgment
of the scientific staff of the National Air
Pollution Control Administration of the ef-
fects that may occur when various levels of
photochemical oxidants are reached in the
ambient air. The more detailed information
from which the conclusions were derived, and
the qualifications that entered- into the con-
sideration of these data, can be found in the
appropriate chapter of this document.
1. Human Exposure
a. Ozone
(1) Long-term exposure of
human subjects.
(a) Exposure to a concentration of up to
390 /ig/m3 (0.2 ppm) for 3 hours a
day, 6 days a week, for 12 weeks, has
not produced any apparent effects
(Chapter 8, section B.2.)
(b) Exposure to a concentration of 980
/Ltg/m3 (0.5 ppm) for 3 hours a day,
6 days a week, has caused a decrease
in the 1-second forced expiratory
volume (FEVli0) after 8 weeks
(Chapter 8, section B.2)
(2) Short-term exposure of
human subjects.
(a) Exposure to a concentration of 40
Mg/m3 (0.02 ppm) was detected
immediately by 9 of 10 subjects.
10-9
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After an average of 5 minutes expo-
sure, subjects could no longer detect
ozone (Chapter 8, section E.2).
(b) Exposure to a concentration of 590
jug/m3 (0.3 ppm) for 8 hours appears
to be the threshold for nasal and throat
irritation (Chapter 8, section E.2.)
(c) Exposure to concentrations of from
1,180 to 1,960 jug/m3 (0.6 to 1.0
ppm) for 1 to 2 hours may impair
pulmonary function by causing in-
creased airway resistance, decreased
carbon monoxide diffusing capacity,
decreased total capacity, and de-
creased forced expiratory volume
(Chapter 8, section B.2'.)
(d) Exposure to concentrations of from
1,960 to 5,900 Mg/m3 (1.0 to 3.0
ppm) for 10 to 30 minutes is in-
tolerable to some people (Chapter 5,
section B.2.)
(e) Exposure to a concentration of
17,600 Mg/m3 (9.0 ppm) produces
severe illness (Chapter 5, section B.2.)
b. Oxidants
(1) Long-term exposure of human
subjects.
Exposure to ambient air containing an
oxidant concentration of about 250
/ig/m3 (0.13 ppm) (maximum daily
value) has caused an increase in the
number of asthmatic attacks in about 5
percent of a group of asthmatic patients.
Such a peak value would be expected to be
associated with a maximum hourly average
concentration of 100 to 120jug/m3 (0.05
to 0.06 ppm) (Chapter 9, section B.3.)
(2) Short-term exposure of
human subjects.
(a) Exposure to an atmosphere with peak
oxidant concentrations of 200 /ig/m3
(0.1 ppm) and above has been asso-
ciated with eye irritation. Such a peak
concentration would be expected to
be associated with a maximum hourly
average concentration of 50 to 100
/zg/m3 (0.025 to 0.05 ppm) (Chapter 9,
section B.3.)
(b) Exposure to an atmosphere with aver-
age hourly oxidant concentrations
ranging from 60 to 590 Mg/m3 (0.03 to
0.30 ppm) has been associated with
impairment of performance of stu-
dent athletes (Chapter 9, section B.4.)
2. Other Exposures
a. Photochemical Oxidants
(1) Effects on vegetation and
laboratory animals.
(a) Exposure to concentrations of about
60 Mg/m3 (0.03 ppm) ozone for 8
hours or to 0.01 ppm peroxyacetyl
nitrate for 5 hours has been associa-
ted with the occurence of leaf lesions
in the most sensitive species, under
laboratory conditions (Chapter 6, sec-
tion E.)
(b) Exposure to ambient air containing
oxidant concentrations of about 100
Mg/m3 (0.05 ppm) for 4 hours has
been associated with leaf injury to the
most sensitive species (Chapter 6,
section E.)
(c) Experimental exposures of laboratory
animals to ozone concentrations of
from 160 to 2,550 MS/m3 (0.08 to
1.30 ppm) for 3 hours has resulted in
increased susceptibility to bacterial
infection (Chapter 8, section B.I.)
b. Ozone Effects on Susceptible Materials
(1) Polymers.
(a) Many polymers, especially rubber, are
extremely sensitive to very small con-
centrations. To provide protection,
antiozonant additives are used, but are
expensive and add to the cost of the
end product (Chapter 7).
(2) Cellulose and dyes.
(a) The cellulose in fabrics is attacked by
ozone, with subsequent weakening of
the fabric. Similarly, certain dyes are
susceptible to fading during exposure
to ozone (Chapter 7). Tables 10-2
10-10
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Table 10-2. EFFECTS OF OZONE
Effect
Vegetation damage2
Cracking of stretched rubber
Odoi detection
Increased susceptibility of
laboratory animals to
bacterial infection
Respiratory irritation (nose
and throat), chest constriction
Changes in pulmonary function:
Diminished FEVj Q after
8 weeks
Small decrements in VC, FRC,
and DL^jQ in, respectively ,3,
2, and 1 out of 7 subjects
Impaired diffusion
capacity (DL^Q)
Increased airway resistance
Reduced VC, severe cough,
inability to concentrate
Acute pulmonary edema
Exposure
ppm
0.03
0.02
0.02
0.08
to
1.30
0.30
0.50
0.20
to
0.30
0.60
to
0.80
0.10
to
1.00
2.00
9.00
ttgjm3
60
40
40
160
to
2,550
590
980
390
to
590
1,180
to
1,570
200
to
1,960
3,900
17,600
Duration
8 hours
1 hour
<5 minutes
3 hours
Continuous during
working hours
3 hours/day,
6 days/week, for
12 weeks
Continuous during
working hours
2 hours
1 hour
2 hours
Unknown
Comment
Sensitive species; laboratory conditions
Vulcanized natural rubber
Odor detected in 9 of 10 subjects
Demonstrated in mice at 160 fig/m
and in mice at 2550 Mg/m3
Occupational exposure of welders,
other pollutants probably also present
Experimental exposure of 6 subjects.
Change returns to normal 6 weeks after
exposure. No changes observed at 390^g/m3
(0.2 ppm)
Occupational exposure. All 7 subjects
smoked. Normal values for VC, FRC, and
DLCO based on predicted value.
Experimental exposure of 11 subjects
Significant increase in 2 of 4 subjects
at 200 Mg/m3 (0.1 ppm) and 4 of 4 subjects
at 1960Mg/m3(1.0ppm)
High temperatures. One subject.
Refers to peak concentration of occupa-
tional exposure. Most of exposure was
to lower level
Reference
Heck and Dunning
Bradley and
Haagen-Smit
Henschler et al.
Coffin et al.
Miller et al.
Kleinfeld et al.
Bennett
Young et al.
Young et al.
Goldsmith et al.
Griswold et al.
Kleinfeld et al.
Similar vegetation damage also occurs upon exposure to 0.01 ppm peroxyacetyl nitrate for 5 hours.
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o
to
Table 10-3. EFFECTS ASSOCIATED WITH OXIDANT CONCENTRATIONS IN PHOTOCHEMICAL SMOG
Effect
Vegetation damage
Eye irritation
Aggravation of respiratory
diseases- asthma
Impaired performance of stu-
dent athletes
Exposure,
ppm
0.05
Mg/m3
100
Exceeding
0.1
0.13a
0.03
to
0.30
200
250
60
to
590
Duration
4 hours
Peak values
Maximum daily
value
1 hour
Comment
Leaf injury to sensitive species
Result of panel response.
Such a peak value would be expected
to be associated with a maximum
hourly average concentration of
50 to 100 Mg/m3 (0.025 to 0.05 ppm)
Patients exposed to ambient air. Value
refers to oxidant level at which number
of attacks increased
Such a peak value would be expected to
be associated with a maximum hourly
average concentration of 100 to 120
Mg/m (0.05 to 0.06 ppm).
Exposure for 1 hour immediately prior
to race
Reference
MacDowall et al
Renzetti and Gobran
Schoettlin and
Landau
Wayne et al.
^Calculated from a measured value of 0.25 ppm (phenolphthalein method) which is equivalent to 0.13 ppm by the KI method.
-------
and 10-3 present these conclusions in
tabular form.
L. RESUME'
Under the conditions prevailing in the areas
where studies were conducted, adverse health
effects, as shown by impairment of perfpr-
mance of student athletes, occurred over a
range of hourly average oxidant concentra-
tions from 60 to 590 jug/m3 (0.03 to 0.3
ppm). An increased frequency of asthma
attacks in a small proportion of subjects with
this disease was shown on days when oxidant
concentrations exceeded peak values of 250
jug/m3 (0.13 ppm), a level that would be
associated with an hourly average concentra-
tion ranging from 100 to 120jug/m3 (0.05 to
0.06 ppm). Adverse health effects, as mani-
fested by eye irritation, were reported by
subjects in several studies when photochemi-
cal oxidant concentrations reached instan-
taneous levels of about 200 pg/m3 (0.10
ppm), a level that would be associated with an
hourly average concentration ranging from 60
to 100 jug/m3 (0.03 to 0.05 ppm).
Adverse effects on sensitive vegetation were
observed from exposure to photochemical
oxidant concentrations of about 100 /ug/m3
(0.05 ppm) for 4 hours. Adverse effects on
materials from exposure to photochemical
oxidants have not been precisely quantified,
but have been observed at the levels presently
occurring in many urban atmospheres.
It is reasonable and prudent to conclude
that, when promulgating ambient air quality
standards, consideration should be given to
requirements for margins of safety that would
take into account possible effects on health,
vegetation, and materials that might occur
below the lowest of the above levels.
10-13
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AP-63
ERRATA FOR
AIR QUALITY CRITERIA FOR PHOTOCHEMICAL OXIDANTS
(Summary and Conclusions)
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oxidant values ot 4yu ug/m^ (u.tb ppmj, wnich might be expected in
relation to a maximum hourly average level as low as 300 ug/m3 (0.15 ppm)
have been associated with aggravation of asthma."
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